Protective effect of rosiglitazone on liver injury in rats with severe acute pancreatitis
10.3760/cma.j.issn.1671-0282.2010.08.020
- VernacularTitle:罗格列酮对重症急性胰腺炎大鼠肝脏的保护作用
- Author:
Xiaoyan CHEN
;
Weixing WANG
;
Youming DING
;
Tao YIN
;
Zhoujun CUI
;
Jia YU
- Publication Type:Journal Article
- Keywords:
Rosiglitasone;
Severe acute pancreatitis;
Liver injury;
High mobility group box-1 protein;
Nuclear factor-kappa B;
Reverse transcription-polymerase chain reaction;
Westem blotting
- From:
Chinese Journal of Emergency Medicine
2010;19(8):847-850
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the therapeutic effects of peroxisome proliferator activating receptor γagonist-rosiglitazone on HMGB1 expression in liver tissue of rats with SAP. Method A hundred and twenty Wistar rats were randomly (random number) divided into the sham operation group(SO group, n = 20) ,SAP group ( n=80) and ROSI treatment group (n =20). SAP group were randomly further divided into the 3 h, 6h, 12 h and 24h subgroups with 20 rats in each group. SAP model was made by retrograde injection of 5 % sodium deoxycholate into the biliopancreatic duct. The serum amylase, AST and ALT, and pathological scores of pancreas and liver tissue were observed. The expression of NF-κB mRNA and the level of HMGB1 protein were investigated respectively by Reverse transcription polymerase chain reaction (RT-PCR) and Westem blot method, respectively. SPSS 16.0software was used to make one-way ANOVA, q -test and correlation analysis. Results Serum amylase, AST and ALT, and pathological scores of pancreas and liver tissue, and the level of HMGB1 protein were markedly increased in each subgroup of SAP compared with SO group ( P ＜ 0.01). The level of HMGB1 protein was positively correlated with the changes of AST, ALT and pathological scores of pancreas and liver tissue. Correlation was not found between HMGB1 and amylase. Treatment with ROSI could significantly reduce the expression of NF-κB mR-NA and the levels of HMGB1 protein, serum AMY, AST and ALT, and pathological scores of pancreas and liver tissue in comparison with 24 h subgroup of SAP (P ＜0.01). Conclusions As a late-acting mediator of inflammation, HMGB1 was involved in the pathophysiological process of SAP-related liver injury. ROSI can reduce the liver injury by inhibition of the expression of the HMGB1.
